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    Oxidatively damaged DNA and its repair after experimental exposure to wood smoke in healthy humans.

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    Authors
    Danielsen, Pernille Hogh
    Brauner, Elvira Vaclavik
    Barregard, Lars
    Sallsten, Gerd
    Wallin, Maria
    Olinski, Ryszard
    Rozalski, Rafal
    Moller, Peter
    Loft, Steffen
    Issue Date
    2008-07-03
    
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    Abstract
    Particulate matter from wood smoke may cause health effects through generation of oxidative stress with resulting damage to DNA. We investigated oxidatively damaged DNA and related repair capacity in peripheral blood mononuclear cells (PBMC) and measured the urinary excretion of repair products after controlled short-term exposure of human volunteers to wood smoke. Thirteen healthy adults were exposed first to clean air and then to wood smoke in a chamber during 4h sessions, 1 week apart. Blood samples were taken 3h after exposure and on the following morning, and urine was collected after exposure, from bedtime until the next morning. We measured the levels of DNA strand breaks (SB), oxidized purines as formamidopyrimidine-DNA-glycosylase (FPG) sites and activity of oxoguanine glycosylase 1 (hOGG1) in PBMC by the comet assay, whereas mRNA levels of hOGG1, nucleoside diphosphate linked moiety X-type motif 1 (hNUDT1) and heme oxygenase 1 (hHO1) were determined by real-time RT-PCR. The excretion of 8-oxo-7,8-dihydro-oxoguanine (8-oxoGua) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in urine was measured by high performance liquid chromatography purification followed by gas chromatography with mass spectrometry. The morning following exposure to wood smoke the PBMC levels of SB were significantly decreased and the mRNA levels of hOGG1 significantly increased. FPG sites, hOGG1 activity, expression of hNUDT1 and hHO1, urinary excretion of 8-oxodG and 8-oxoGua did not change significantly. Our findings support that exposure to wood smoke causes systemic effects, although we could not demonstrate genotoxic effects, possibly explained by enhanced repair and timing of sampling.
    Citation
    Mutat. Res. 2008, 642 (1-2):37-42
    Journal
    Mutation Research
    URI
    http://hdl.handle.net/10146/33832
    DOI
    10.1016/j.mrfmmm.2008.04.001
    PubMed ID
    18495177
    Additional Links
    http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T2C-4S8TBCC-1&_user=1843694&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000055040&_version=1&_urlVersion=0&_userid=1843694&md5=de3e96633626fd29ec3c50d8b64cadb3
    Type
    Article
    Language
    en
    ISSN
    0027-5107
    Sponsors
    Pernille Hogh Danielsen, Elvira Vaclavik Brauner, Ryszard Olinski, Rafal Rozalski, Peter Moller and Steffen Loft are partners in ECNIS (Environmental Cancer Risk, Nutrition and Individual Susceptibility), a network of excellence operating within the European Union 6th Framework Program, Priority 5: “Food Quality and Safety” (Contract No. 513943).
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.mrfmmm.2008.04.001
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